Case report no. 1, Department Pathological Physiology V. Danzig, MD, PhD, 2nd Dept. Internal Medicine Cardiology and Angiology Division 1st Med.F CUNI

Patient history 78 yr. old male, retiree, worked as mechanical engineer Family history: longevity, cardiovascular complications, yet no early deaths (Ab)usus: quitted smoking 15 yrs ago, 10-15 cigarettes daily before, alcohol drinking denies Patient history: repeated herniotomy, benign prostatic hypetrophy, diabetes mellitus last 6 years – on diet

Patient history - questions What is the risk (high/ medium/ low) of cardiovascular disease in this 78 year old former smoker? When is the onset of cardiovascular disorder considered early and when timely? What are the effects of smoking on the cardiovascular system and on the respiratory system (related to malignant tumors), what are the differences?

Current disorder Last 3 years progression of exertional dyspnea and chest pain projecting to medium and lower sternum Progressive worsening last 2 weeks, pains in rest Once a pain attack in walking, loss of consciousness, awakened lying on ground Admitted to hospital after a nigh long lasting retro-sternal pains, dyspnea, felt forced to sit, first time felt as well irregular and fast heardbeats

Current disorder - questions Give clinical definition of dyspnea. What is its origin in (left) heart disorder? Other causes besides cardiomyopathy? Name/ description: ischemic myocardial pain, its mechanism/ cause? Name/ description: of a short time loss of consciousness What is the prime cause of myocardial ischemia in Czech population? What is differential diagnostics? Synonyms for palpitations? They are signs of what diseases? What does it mean when patient complains that they are irregular?

What investigation methods to use in this patient ECG: - what are signs of acute myocardial infarction? Elevations of the ST segment? - cardiac rhythm ? Biochemical markers – in this patient were not elevated – no myocardial necrosis X-ray of heart and lungs – venostasis (oedema)

ECG at admission

Next: atrial fibrillation w. wide QRS complexes

Definition of atrial fibrillation Atrial fibrillation is an irregular atrial activity. ECG record shows no P waves. Instead there are fast oscillations, also denoted as “F” waves. Ventricular response are typically QRS complexes with RR intervals of different length.

Investigation methods - questions How many leads are in standard ECG? Names and groups of leads? How we record continuous ECG and how many leads in it we use? Name biochemical cardiac markers, describe them, what is their use? What are signs of atrial fibrillation? What are the risks?

Further investigations echokardiography, ECHO: - Findings: calcified aortal valve with limited cusp excursions, Doppler – tight stenosis w. gradients 65/ 34 mm Hg, mouth area 0.4 cm2/m2 (per body surface) - Ascendent aorta dilation - dilatace ascendentní aorty - EF (ejection fraction) LV 0,45 – 0,49 (= 45-49%) selective coronarography: no pathology/ normal findings

ECHO – morphological investigation

ECHO – continuous Doppler

Cathetrisation record – aortal stenosis

Further investigations - questions What gradient is important here (related to aortal valve and its stenosis) What are two basic approaches to measure the gradient? Compare the two? Can we always use both of them? What can be the complications? Why we calculate the area? Explain cases when area is significantly reduced yet the high gradient is not present. What is left ventricle ejection fraction, its units and normal values?

Therapy Temporary therapy: aim to compensate – therapy of heart failure and control of ventricular response to atrial fibrillation Definitive therapy: replacement of aortal valve by bio-prosthesis, eventually a plastic surgery of ascendent aorta

Therapy - questions What is the relation of atrial fibrillation to the principal heart disorder (aortal stenosis)? Why as a first step in the therapy of atrial fibrillation we need a slow down of the ventricular frequency? Why and when a plastic surgery of aorta is needed as well?

Conclusions I Aortal stenosis: is frequent and becoming yet more frequent acquired valve disorder, as the population is ageing. This condition is followed up by a pressure overload of left ventricle. This propagates backwards and leads to atrial dilation (closing a vicious circle this way) and back to pulmonary circulation. Typical compensatory mechanism is left ventricle hypertrophy. This is followed up by development of ventricle dilation, deterioration of systolic function and failure.

Conclusions II Symptomes and their patho-physiological explanations (Q/+A): dyspnoe by back-propagation of elevated intra-ventricular pressure stenocardia lowered throughput in coronary arteries, esp. in tachycardia exertional syncope inability to elevate cardiac output when valve mouth area is reduced low pressure amplitude slower onset of systolic pressure in aorta Therapy: aortal valve replacement (bio-prosthesis) by cardio-surgery. Transcatheter Aortic Valve Implantation in selected high risk patients.